|
|
Prepublished online as a Blood First Edition Paper on July 5, 2002; DOI 10.1182/blood-2002-02-0626.
 Previous Article | Table of Contents | Next Article 
Blood, 15 November 2002, Vol. 100, No. 10, pp. 3790-3796
RED CELLS
Heparin inhibits the flow adhesion of sickle red blood cells to
P-selectin
Neil M. Matsui,
Ajit Varki, and
Stephen H. Embury
From the Department of Pediatrics and the
Department of Medicine, University of California-San Francisco, San
Francisco General Hospital, and the Northern California Comprehensive
Sickle Cell Center, San Francisco; and the Glycobiology Research and
Training Center, Departments of Medicine and Cellular and Molecular
Medicine, University of California-San Diego, La Jolla.
The adhesion of sickle erythrocytes to vascular endothelium is
important to the generation of vascular occlusion. Interactions between
sickle cells and the endothelium use several cell adhesion molecules.
We have reported that sickle cell adhesion to endothelial cells under
static conditions involves P-selectin. Others have shown that sickle
cell adhesion is decreased by unfractionated heparin, but the molecular
target of this inhibition has not been defined. We postulated that the
adhesion of sickle cells to P-selectin might be the pathway blocked by
unfractionated heparin. In this report we demonstrate that the flow
adherence of sickle cells to thrombin-treated human vascular
endothelial cells also uses P-selectin and that this component of
adhesion is inhibited by unfractionated heparin. We also demonstrate
that sickle cells adhere to immobilized recombinant P-selectin under
flow conditions. This adhesion too was inhibited by unfractionated
heparin, in a concentration range that is clinically attainable. These
findings and the general role of P-selectin in initiating adhesion of
blood cells to the endothelium suggest that unfractionated heparin may be useful in preventing painful vascular occlusion. A clinical trial to
test this hypothesis is indicated.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
R. Zennadi, B. J. Moeller, E. J. Whalen, M. Batchvarova, K. Xu, S. Shan, M. Delahunty, M. W. Dewhirst, and M. J. Telen
Epinephrine-induced activation of LW-mediated sickle cell adhesion and vaso-occlusion in vivo
Blood,
October 1, 2007;
110(7):
2708 - 2717.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. M. Finnegan, G. A. Barabino, X.-d. Liu, H.-Y. Chang, A. Jonczyk, and D. K. Kaul
Small-molecule cyclic {alpha}Vbeta3 antagonists inhibit sickle red cell adhesion to vascular endothelium and vasoocclusion
Am J Physiol Heart Circ Physiol,
August 1, 2007;
293(2):
H1038 - H1045.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. J. Telen
Role of Adhesion Molecules and Vascular Endothelium in the Pathogenesis of Sickle Cell Disease
Hematology,
January 1, 2007;
2007(1):
84 - 90.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. I. Ataga and N. S. Key
Hypercoagulability in Sickle Cell Disease: New Approaches to an Old Problem
Hematology,
January 1, 2007;
2007(1):
91 - 96.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. L. Stevenson, S. H. Choi, and A. Varki
Differential Metastasis Inhibition by Clinically Relevant Levels of Heparins--Correlation with Selectin Inhibition, Not Antithrombotic Activity
Clin. Cancer Res.,
October 1, 2005;
11(19):
7003 - 7011.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. H. Embury, N. M. Matsui, S. Ramanujam, T. N. Mayadas, C. T. Noguchi, B. A. Diwan, N. Mohandas, and A. T. W. Cheung
The contribution of endothelial cell P-selectin to the microvascular flow of mouse sickle erythrocytes in vivo
Blood,
November 15, 2004;
104(10):
3378 - 3385.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. R. Buchanan, M. R. DeBaun, C. T. Quinn, and M. H. Steinberg
Sickle Cell Disease
Hematology,
January 1, 2004;
2004(1):
35 - 47.
[Abstract]
[Full Text]
[PDF]
|
|
|
| |
